mTORC2 controls actin polymerization required for consolidation of long-term memory
What this study shows
Conditional deletion of Rictor in the postnatal mouse forebrain reduced mTORC2 activity and selectively impaired long-term memory and the late phase of hippocampal LTP, with a comparable long-term-memory deficit in dTORC2-deficient flies. Hippocampal actin polymerisation was reduced, and restoring it rescued both L-LTP and long-term memory; a compound that raised mTORC2 activity converted early LTP into late LTP and enhanced memory. This is the loss-of-function AND rescue evidence that mTORC2 is required for memory consolidation - the arm chronic rapamycin also disrupts, and the study Open Question H8 needs for its mTORC2 liability leg, which until 2026-09-05 rested on no supporting study at all.
At a glance
| Evidence type | A Animal model Marked A because it is an animal intervention or observation study measuring an organismal outcome (model: Conditional Rictor-knockout mice (postnatal forebrain) and Drosophila); the code names the system studied -- animal work can be rigorous and still not be human data. |
| Study type | 4 - Animal Study |
| Model system | Conditional Rictor-knockout mice (postnatal forebrain) and Drosophila |
| Journal | Nature Neuroscience |
| Year | 2013 |
| Peer reviewed | — |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1038/nn.3351 · PMID 23455608 · Free full text (PMC3615448) |
Extracted findings
These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.
| Intervention | Conditional postnatal forebrain Rictor deletion; dTORC2-deficient flies; actin-polymerisation rescue; mTORC2-activating compound |
| Target | mTORC2 / Rictor; actin polymerisation |
| Model | Mouse; Drosophila |
| Effect | Rictor deletion impairs long-term memory and late-phase LTP; restoring actin polymerisation rescues both |
In the Atlas
Related topics
Links in the pathway map
- Supports mTORC2 activates Actin cytoskeleton
- Supports Rictor required-for mTORC2
Open questions that cite this study
- Cited as supporting evidence for the open question Brain-penetrant mTOR inhibition clears aggregates in models, but human dosing has not been shown to reach the brain — and mTORC2 is needed for memory in mice.
More studies on this topic
- Rictor, a novel binding partner of mTOR, defines a rapamycin-insensitive and raptor-independent pathway that regulates the cytoskeleton (2004)
- Mammalian TOR complex 2 controls the actin cytoskeleton and is rapamycin insensitive (2004)
- Two TOR complexes, only one of which is rapamycin sensitive, have distinct roles in cell growth control (2002)
- Translational control of long-lasting synaptic plasticity and memory (2009)
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